14659
2016
eng
3
8
article
7th NEUROWIND e.V. scientific meeting
1
2017-03-31
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Report on the 7th scientific meeting of the Association for the Advancement of Young Academics in Neurology (NEUROWIND e.V.) held in Motzen, Germany, October 30–November 1, 2015
From October 30–November 1, 2015, the 7th NEUROWIND e.V. meeting was held in Motzen, Brandenburg, Germany. Seventy doctoral students and postdocs from over 25 different groups working in German and Swiss University Hospitals or Research Institutes attended the meeting to discuss their latest experiments and findings in the fields of neuroimmunology, neurodegeneration and neurovascular research. This meeting report summarizes the many diverse presentations and the new preclinical to clinical neurology research data that were shared by the participants at the meeting.
Experimental and Translational Stroke Medicine
10.1186/s13231-016-0017-y
urn:nbn:de:bvb:20-opus-146595
Experimental and Translational Stroke Medicine (2016) 8:3 DOI 10.1186/s13231-016-0017-y
Thomas Korn
Christoph Kleinschnitz
Tim Magnus
Sven G. Meuth
Ralf A. Linker
eng
uncontrolled
NEUROWIND
Medizin und Gesundheit
open_access
Neurologische Klinik und Poliklinik
Förderzeitraum 2016
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/14659/Korn_10.1186_s13231-016-0017-y.pdf
16550
2016
eng
11626
7
article
1
2018-07-24
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Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells
Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells. Immune activation by FXII is mediated by dendritic cells in a CD87-dependent manner and involves alterations in intracellular cyclic AMP formation. Our study demonstrates that a member of the plasmatic coagulation cascade is a key mediator of autoimmunity. FXII inhibition may provide a strategy to combat MS and other immune-related disorders.
Nature Communications
10.1038/ncomms11626
urn:nbn:de:bvb:20-opus-165503
Nature Communications, 2015, 7:11626. DOI: 10.1038/ncomms11626
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Kerstin Göbel
Susann Pankratz
Chloi-Magdalini Asaridou
Alexander M. Herrmann
Stefan Bittner
Monika Merker
Tobias Ruck
Sarah Glumm
Friederike Langhauser
Peter Kraft
Thorsten F. Krug
Johanna Breuer
Martin Herold
Catharina C. Gross
Denise Beckmann
Adelheid Korb-Pap
Michael K. Schuhmann
Stefanie Kuerten
Ioannis Mitroulis
Clemens Ruppert
Marc W. Nolte
Con Panousis
Luisa Klotz
Beate Kehrel
Thomas Korn
Harald F. Langer
Thomas Pap
Bernhard Nieswandt
Heinz Wiendl
Triantafyllos Chavakis
Christoph Kleinschnitz
Sven G. Meuth
eng
uncontrolled
blood coagulation
eng
uncontrolled
factor XII
eng
uncontrolled
neuroinflammation
eng
uncontrolled
dendric cells
Biowissenschaften; Biologie
Medizin und Gesundheit
open_access
Institut für Anatomie und Zellbiologie
Neurologische Klinik und Poliklinik
Rudolf-Virchow-Zentrum
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/16550/Goebel_Nature_Communications.pdf